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Finals > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

how can you differentiate biliary colic from acute cholangitis

A

In contrast to acute cholecystitis, there is no fever and inflammatory markers are normal in biliary colic

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2
Q

what is charcot’s triad

A
  • it is
    • right upper quadrant pain
    • fever
    • jaundice
  • it’s for ascending cholangiti
  • it occurs in ~20-50% of people with ascending cholangitis
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3
Q

is pain from duodenal ulcers or gastric ulcers made worse by eating

A

Duodenal ulcers: more common than gastric ulcers, epigastric pain relieved by eating

Gastric ulcers: epigastric pain worsened by eating

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4
Q

what is rovsing’s sign?

A

more pain in RIF than LIF when palpating LIF

it indicates appendicitis

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5
Q

when would you get tinkling bowel sounds

A

if there is intestinal obstruction

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6
Q

how does the pain differ between renal colic and acute pyelonephritis

A
  • renal colic:
    • Pain is often severe but intermittent. Patient’s are characteristically restless
    • Visible or non-visible haematuria may be present
  • acute pyelonephritis:
    • Fever, vomiting and rigors
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7
Q

what is the most common causative organism in ascending cholangitis

A

E. coli

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8
Q

what is reynold’s pentad for ascending cholangitis

A
  • it’s charcot’s triad:
    • fever
    • RUQ pain
    • jaundice
  • plus hypotension and confusion

it’s for ascending cholangitis

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9
Q

how do you diagnose ascending cholangitis

A

ultrasound is generally used first-line in suspected cases to look for bile duct dilation and bile duct stones

bloods will show raised white cells and raised inflammatory markers

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10
Q

what is the management of ascending cholangitis

A

intravenous antibiotics

endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction

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11
Q

clincal features of acute pancreatitis

A

severe epigastric pain that may radiate through to the back

vomiting is common

examination may reveal epigastric tenderness, ileus and low-grade fever

periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare

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12
Q

how do you diagnose pancreatitis

A

a diagnosis of acute pancreatits can be made without imaging if characteristic pain + amylase/lipase > 3 times normal level

however, early ultrasound imaging is important to assess the aetiology as this may affect management - e.g. patients with gallstones/biliary obstruction

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13
Q

what are the two important blood tests for pancreatitis

A
  • serum amylase
    • raised in 75% of patients
    • typically > 3 times the upper limit of normal in pancreatitis
    • levels do not correlate with disease severity
    • specificity about 90%
  • serum lipase
    • more sensitive and specific than serum amylase
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14
Q

what are the non-pancreatitis causes of raised amylase

A

pancreatic pseudocyst

mesenteric infarct

perforated viscus

acute cholecystitis

diabetic ketoacidosis

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15
Q

what are some poor prognostic factors in pancreatitis

A
  • age > 55 years
  • hypocalcaemia
  • hyperglycaemia
  • hypoxia
  • neutrophilia
  • elevated LDH and AST
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16
Q

what are the causes of pancreatitis

A
  • GETSMASHED
    • Gallstones
    • Ethanol
    • Trauma
    • Steroids
    • Mumps (other viruses include Coxsackie B)
    • Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
    • Scorpion venom
    • Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
    • ERCP
    • Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)
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17
Q

how do you classify the severity of pancreatitis

A
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18
Q

management of pancreatitis

A
  • fluids
    • aggressive early rehydration with crystalloids
    • aim for urine output of 0.5ml/kg/hr
    • may relieve pain by treating lactic acidosis
  • analgesia
    • IV opioids
  • nutrition
    • don’t make them nil by mouth unless they are vomiting
    • enteral nutrition should be offered to anyone with moderately severe or severe acute pancreatitis within 72 hours of presentation
    • parenteral nutrition only used if enteral fails
  • surgery
    • if due to gallstones then cholecystectomy
    • if obstructed biliary system due to stones then ERCP
    • if infected necrosis then either radiological drainage or surgical necrosectomy.
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19
Q

what is the main cause of chronic pancreatitis

A
  • 80% of cases are due to excess alcohol use
  • 20% of cases are due to:
    • genetic: cystic fibrosis, haemochromatosis
    • ductal obstruction: tumours, stones,
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20
Q

clinical features of chronic pancreatitis

A
  • pain is typically worse 15 to 30 minutes following a meal
  • steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
  • diabetes mellitus develops in the majority of patients typically more than 20 years after symptom begin
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21
Q

how do you investigate chronic pancreatitis

A
  • CT shows pancreatic calcification
  • faecal elastase detects pancreatic exocrine function
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22
Q

management of chronic pancreatitis

A

pancreatic enzyme supplementation

analgesia

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23
Q

is there a vaccine for hepatitis C

A

no

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24
Q

what is the investigation to diagnose hepatitis C

A

HCV RNA

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25
Q

is hepatitis C acute or chronic

A
  • around 15-45% of patients will clear the virus after an acute infection (depending on their age and underlying health) and hence the majority (55-85%) will develop chronic hepatitis C
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26
Q

what is the definition of chronic hepatitis C

A

the persistence of HCV RNA in the blood for 6 months.

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27
Q

complications of chronic hepatitis C infection

A
  • cirrhosis
  • hepatocellular carcinoma
  • membranoproliferative glomerulonephritis
  • sjorgen’s syndrome
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28
Q

how do you manage hepatitis C

A
  • daclatasvir + sofosbuvir or sofosbuvir + simeprevir with or without ribavirin
  • aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
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29
Q

what are the side effects of ribavirin

A

haemolytic anaemia

cough

Women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic

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30
Q

what is hepatitis D and B coinfection

A

A patient is infected with hepatitis B and hepatitis D at the same time

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31
Q

what is hepatitis B and D superinfection

A

A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection

Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.

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32
Q

what is the treatment for hepatitis B

A

pegylated interferon-alpha

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33
Q

important things to remember about hep E

A
  • faecal oral route
  • incubation period is 3-8 weeks
  • common in Central and South-East Asia, North and West Africa, and in Mexico
  • causes significant mortality in pregnancy (20%)
  • does not cause chronic disease
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34
Q

how long is the incubation period for hepatitis A

A

2-4 weeks

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35
Q

what are the clinical features of hepatitis A

A
  • flu-like prodrome
  • abdominal pain: typically right upper quadrant
  • tender hepatomegaly
  • jaundice
  • cholestatic liver function tests
  • faecal-oral spread
  • doesn’t cause chronic disease
  • benign, self-limiting disease
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36
Q

who should be vaccinated against hepatitis A

A
  • an effective vaccine is available
  • after the initial dose a booster dose should be given 6-12 months later
  • people travelling to or going to reside in areas of high or intermediate prevalence, if aged > 1 year old
  • people with chronic liver disease
  • patients with haemophilia
  • men who have sex with men
  • injecting drug users
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37
Q

how will lfts be deranged in alcoholic liver disease

A
  • cGamma-GT will be raised
  • the AST-ALT ration will be >2
    • if it’s >3 then this is strongly suggestive of acute alcoholic hepatitis
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38
Q

what can be used to treat alcoholic hepatitis

A

prednisolone

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39
Q

which weird blood test can show hepatocellular carcinoma

A

raised AFP can be a useful diagnostic marker of HCC

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40
Q

Who should be screened for hepatocellular carcinoma and how

A
  • Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
    • patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
    • men with liver cirrhosis secondary to alcohol
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41
Q

a serum-ascites albumin gradient above what level is indicative of portal hypertension

A

11g/L

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42
Q

what are some causes of a serum-ascites albumin gradient >11g/L

A
  • Liver disorders are the most common cause
    • cirrhosis/alcoholic liver disease
    • acute liver failure
    • liver metastases
  • Cardiac
    • right heart failure
    • constrictive pericarditis
  • Other causes
    • Budd-Chiari syndrome
    • portal vein thrombosis
    • veno-occlusive disease
    • myxoedema
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43
Q

what is saag

A

serum-asites albumin gradient

SAAG = (serum albumin) − (albumin level of ascitic fluid).

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44
Q

what are some causes of saag <11g/L

A
  • Hypoalbuminaemia
    • nephrotic syndrome
    • severe malnutrition (e.g. Kwashiorkor)
  • Malignancy
    • peritoneal carcinomatosis
  • Infections
    • tuberculous peritonitis
  • Other causes
    • pancreatitisis
    • bowel obstruction
    • biliary ascites
    • postoperative lymphatic leak
    • serositis in connective tissue diseases
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45
Q

management of ascites

A
  • sodium restriction
  • if sodium <124 then consider fluid restriction
  • spironolactone +/- loop diuretic
  • therapeutic paracentesis of tense ascites
    • if >5L then give albumin cover to prevent paracentesis induced circulatory dysfunction
  • transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
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46
Q

which patients with ascites should get prophylactic antibiotic cover and what should they have

A

prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved

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47
Q

how do you diagnose spontaneous bacterial peritonitis

A
  • paracentesis
    • neutrophil count >250 cells/uL
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48
Q

what is the most common causative organism in spontaneous bacterial peritonitis

A

e.coli

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49
Q

what is the best antibiotic for spontaneous bacterial peritonitis

A

IV cefotaxime

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50
Q

what is the pathophysiology of acute colecystitis

A
  • develops secondary to gallstones in 90% of patients (acute calculous cholecystitis)
  • the remaining 10% of cases are referred to as acalculous cholecystitis
    • typically seen in hospitalised and severely ill patients
    • multifactorial pathophysiology: gallbladder stasis, hypoperfusion, infection
    • in immunosuppressed patients it may develop secondary to Cryptosporidium or cytomegalovirus
    • associated with high morbidity and mortality rates
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51
Q

what is the first line investigation for acute cholecystitis

A
  • ultrasound is the first-line investigation of choice
  • if the diagnosis remains unclear then cholescintigraphy (HIDA scan) may be used
    • technetium-labelled HIDA (hepatobiliary iminodiacetic acid) is injected IV and taken up selectively by hepatocytes and excreted into bile
    • in acute cholecystitis there is cystic duct obstruction (secondary to odema associated with inflammation or an obstructing stone) and hence the gallbladder will not be visualised
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52
Q

what is the treatment for acute cholecystitis

A

iv antibiotics and early laparoscopic cholecystectomy within 1 week of diagnosis

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53
Q

risk factors for gallstones

A
  • Fat
  • Female
  • Fertile (pregnancy and COCP)
  • Forty
  • also
    • diabetes
    • crohns
    • rapid weightloss (i.e. from bariatric surgery)
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54
Q

what is the pain in biliary colic caused by

A

gallstones passing through the biliary tree

or due to the gallbladder contracting around a stone

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55
Q

features of biliary colic

A
  • colicky right upper quadrant pain
    • worse after eating
    • may radiate to back, between scapulae
  • nausea and vomiting
  • LFTs are NORMAL
    • unless it’s in the CBD
  • NO FEVER
  • Inflammatory markers are NORMAL
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56
Q

complications of gallstones

A
  • acute cholecystitis: the most common complication
  • ascending cholangitis
  • acute pancreatitis
  • gallstone ileus
  • gallbladder cancer
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57
Q

management of cholangitis

A
  • Fluid resuscitation
  • Broad-spectrum intravenous antibiotics
  • Correct any coagulopathy
  • Early ERCP
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58
Q

how do you manage asymptomatic gallstones

A
  • if in gallbladder then manage expectantly since they rarely cause problems
  • if in cbd then consider surgical managment
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59
Q

what are the two scores for severity of liver cirrhosis

A
  • Child-Pugh score
  • Model for end stage liver disease (MELD)
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60
Q

what are the risks of ERCP

A
  • bleeding
  • cholangitis
  • perforation
  • pancreatitis
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61
Q

What is the model for end stage liver disease

A

Uses a combination of a patient’s bilirubin, creatinine, and the international normalized ratio (INR) to predict survival. A formula is used to calculate the score.

formula is quite long and boring don’t learn it

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62
Q

how do you diagnose liver cirrhosis

A
  • transient elastography
    • brand name ‘Fibroscan’
    • uses a 50-MHz wave is passed into the liver from a small transducer on the end of an ultrasound probe
    • measures the ‘stiffness’ of the liver which is a proxy for fibrosis
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63
Q

what further investigations should you do for people with liver cirrhosis?

A
  • Upper endoscopy to check for varices in patient’s with a new diagnosis of cirrhosis
  • liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
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64
Q

what is the child pugh classification

A
  • it’s for staging liver cirrhosis
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65
Q

which HLA types is coeliac associated with

A

HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).

66
Q

should coeliac testing be done while the patient is taking gluten or not

A

patients should reintroduce gluten for at least 6 weeks prior to testing.

67
Q

what serology can you do for coeliac

A
  • tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
  • endomyseal antibody (IgA)
    • needed to look for selective IgA deficiency, which would give a false negative coeliac result
68
Q

what is the gold standard for diagnosis of coeliac

A
  • endoscopic intestinal biopsy (duodenum or jejumum):
    • villous atrophy
    • crypt hyperplasia
    • increase in intraepithelial lymphocytes
    • lamina propria infiltration with lymphocytes
69
Q

apart from being gluten free what do coeliac patients need

A
  • they might have functional hyposplenism
  • For this reason, they’re offered the pneumococcal vaccine
    • and a booster every 5 years
70
Q

first-line pharmacological treatment of IBS

A
  • pain: antispasmodic agents
  • constipation: laxatives but avoid lactulose
  • diarrhoea: loperamide is first-line
71
Q

what is the second line treatment of IBS

A

low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg)

72
Q

what is the difference between diverticulosis, diverticulitis and diverticular disease

A
  • diverticulosis: outpouchings present without symptoms
  • diverticular disease: symptoms present
  • diverticulitis: infection of the diverticula
73
Q

symptoms of diverticular disease

A
  • Altered bowel habit
  • rectal bleeding
  • Abdominal pain
74
Q

complications of diverticular disease

A
  • Diverticulitis
  • Haemorrhage
  • Development of fistula
  • Perforation and faecal peritonitis
  • Perforation and development of abscess
  • Development of diverticular phlegmon
75
Q

diverticulitis investigation

A
  • FBC: raised WCC
  • CRP: raised
  • Erect CXR: may show pneumoperitoneum in cases of perforation
  • AXR: may show dilated bowel loops, obstruction or abscesses
  • CT: this is the best modality in suspected abscesses
  • Colonoscopy: should be avoided initially due to increased risk of perforation in diverticulitis
76
Q

management of diverticulitis

A
  • mild cases of acute diverticulitis may be managed with oral antibiotics, liquid diet and analgesia
  • if the symptoms don’t settle within 72 hours, or the patient intiially presents with more severe symptoms, the patient should be admitted to hospital for IV antibiotics
77
Q

if patients with dyspepsia don’t meet criteria for referral then how do you treat them

A
    1. Review medications for possible causes of dyspepsia
    1. Lifestyle advice
    1. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
      * if symptoms persist after either of the above approaches then the alternative approach should be tried
78
Q

which patients require urgent referral for endoscopy for investigation of stomach and oesophageal cancer

A
  • All patients who’ve got dysphagia
  • All patients who’ve got an upper abdominal mass consistent with stomach cancer
  • Patients aged >= 55 years who’ve got weight loss, AND any of the following:
    • upper abdominal pain
    • reflux
    • dyspepsia
79
Q

which patients require non urgent referral for endoscopy for investigation of stomach and oesophageal cancer

A
  • Patients with haematemesis
  • Patients aged >= 55 years who’ve got:
    • treatment-resistant dyspepsia or
    • upper abdominal pain with low haemoglobin levels or
    • raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
    • nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
80
Q

what conditions are associated with H. pylori infection

A
  • peptic ulcer disease
    • 95% of duodenal ulcers
    • 75% of gastric ulcers
  • gastric cancer
  • B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
  • atrophic gastritis
81
Q

management of H. pylori infection

A
  • a 7-day course of
    • a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
    • if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
82
Q

how do you diagnose H.pylori infection

A

Urea breath test

  • patients consume a drink containing carbon isotope 13 (13C) enriched urea
  • urea is broken down by H. pylori urease
  • after 30 mins patient exhale into a glass tube
  • mass spectrometry analysis calculates the amount of 13C CO2
  • should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
  • sensitivity 95-98%, specificity 97-98%
  • may be used to check for H. pylori eradication
83
Q

indications for upper GI endoscopy in GORD

A
  • age > 55 years
  • symptoms > 4 weeks or persistent symptoms despite treatment
  • dysphagia
  • relapsing symptoms
  • weight loss
84
Q

how do you treat endoscopically proved oesophagitis

A
  • full dose proton pump inhibitor (PPI) for 1-2 months
  • if response then low dose treatment as required
  • if no response then double-dose PPI for 1 month
85
Q

how do you treat endoscopically negative oesophagitis

A
  • full dose PPI for 1 month
  • if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
86
Q

what is the histological change seen in barrett’s oesophagus

A

squamous epithelium being replaced by columnar epithelium.

87
Q

how can you subdivide barrett’s oesophagus?

A

short (<3cm) and long (>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia

88
Q

management of barrett’s oesophagus

A
  • Endoscopic surveillance
    • for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
  • If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
    • endoscopic mucosal resection
    • radiofrequency ablation
89
Q

management of barrett’s oesophagus

A
  • Endoscopic surveillance
    • for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
  • If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
    • endoscopic mucosal resection
    • radiofrequency ablation
90
Q

what is the inheritance pattern of haemochromatosis

A

autosomal recessive

91
Q

what is the prevalence of haemochromatosis in people of european descent

A

1 in 200, making it more common than cystic fibrosis

92
Q

features of haemochromatosis

A
  • early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
  • ‘bronze’ skin pigmentation
  • diabetes mellitus
  • liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
  • cardiac failure (2nd to dilated cardiomyopathy)
  • hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
  • arthritis (especially of the hands)
93
Q

which features of haemochromatosis are reversible and which are not

94
Q

what do joint x rays show in haemochromatosis

A

Joint x-rays characteristically show chondrocalcinosis

95
Q

what do iron studies show in haemochromatosis

A
  • transferrin saturation > 55% in men or > 50% in women
  • raised ferritin (e.g. > 500 ug/l) and iron
  • low TIBC
96
Q

what are diagnostic tests in haemochromatosis

A
  • transferrin saturation > 55% in men or > 50% in women
  • raised ferritin (e.g. > 500 ug/l) and iron
  • low TIBC
97
Q

what is the management of haemochromatosis

A
  • Venesection is the first-line treatment
    • transferrin saturation should be kept below 50%
    • serum ferritin concentration should be kept below 50 ug/l
  • desferrioxamine may be used second-line
98
Q

where is haemorrhoidal tissue found

A

Haemorrhoidal tissue are vascular cushions that contribute to continence

they are found at 3 o’clock, 7’o’clock and 11 o’clock

99
Q

how do you grade haemorrhoids

100
Q

how do you manage haemorrhoids

A
  • soften stools: increase dietary fibre and fluid intake
  • topical local anaesthetics and steroids may be used to help symptoms
  • rubber band ligation
  • surgery is reserved for large symptomatic haemorrhoids which do not respond to the above
  • newer treatments: Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy
101
Q

how do thrombosed external haemorrhoids present and how do you manage them

A
  • typically present with significant pain
  • examination reveals a purplish, oedematous, tender subcutaneous perianal mass
  • if patient presents within 72 hours then referral should be considered for excision.
  • Otherwise patients can usually be managed with stool softeners, ice packs and analgesia.
  • Symptoms usually settle within 10 days
102
Q

what are the two types of hiatus hernias

A
  • sliding: accounts for 95% of hiatus hernias, the gastroesophageal junction moves above the diaphragm
  • rolling (paraoesophageal): the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
103
Q

management of hiatus hernia

A
  • all patients benefit from conservative management e.g. weight loss
  • medical management: proton pump inhibitor therapy
  • surgical management: only really has a role in symptomatic paraesophageal (rolling) hernias
104
Q

when should you suspect oesophageal rupture

A

in patients with severe chest pain without cardiac diagnosis and signs suggestive of pneumonia without convincing history, where there is history of vomiting

105
Q

investigation and finding of oesophageal rupture

A

Erect CXR shows infiltrate or effusion in 90% of cases

106
Q

causes for dysphagia

107
Q

extrinsic causes of dysphagia

A
  • mediastinal masses
  • cervical spondylosis
108
Q

causes for dysphagia in the oseophageal wall

A
  • Achalasia
  • Diffuse oesophageal spasm
  • Hypertensive lower oesophageal sphincter
109
Q

intrinsic causes of dysphagia

A
  • Tumours
  • Strictures
  • Oesophageal web
  • Schatzki rings
110
Q

neurological causes of dysphagia

A
  • CVA
  • Parkinson’s disease
  • Multiple Sclerosis
  • Myasthenia Gravis
111
Q

six causes of hyposplenism

A
  • splenectomy
  • sickle-cell
  • coeliac disease
  • Graves’ disease
  • systemic lupus erythematosus
  • amyloid
112
Q

what is the difference between acute and chronic diarrhoea

A
  • diarrhoea is > watery stools per day
  • chronic is >14 days
  • acute is <14 days
113
Q

clinical features of infectious mononucleosis

A
  • sore throat
  • pyrexia
  • lymphadenopathy
  • palatal petychia
  • splenomegaly (50%)
  • hepatitis (transient rise in ALT)
  • lymphocytosis
  • maculopapular rash if they take amoxicillin at the same time
114
Q

how long does infectious mononucleosis normally last

A

symptoms usually resolve within 2-4 weeks

115
Q

management of infectious mononucleosis

A
  • supportive
  • lots of fluids
  • lots of analgesia
  • avoid contact sport for 4 weeks after
116
Q

management of infectious mononucleosis

A
  • supportive
  • lots of fluids
  • lots of analgesia
  • avoid contact sport for 4 weeks after
117
Q

why do you get oxalate renal stones in crohns

A

impaired bile acid rebsorption increases the loss calcium in the bile. Calcium normally binds oxalate.

doesn’t happen in UC as bile is reabsorbed in the ileum

118
Q

compare ulcerative colitis in terms of: features, extra-intestinal features, complications, histology, endoscopy and radiology

119
Q

how do you monitor disease activity in crohn’s

120
Q

what would you see on small bowel enema in crohn’s

A
  • high sensitivity and specificity for examination of the terminal ileum
  • strictures: ‘Kantor’s string sign’
  • proximal bowel dilation
  • ‘rose thorn’ ulcers
  • fistulae
121
Q

management of crohn’s

A
  • Stopping smoking is a priority
  • inducing remission
    • glucocorticoids (oral, topical or IV)
    • 5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
  • maintaining remission
    • azathioprine or mercaptopurine is used first-line to maintain remission
  • surgery
    • segmental bowel resections
    • incision and drainage of perianal abscesses
122
Q

what is the peak age of ulcerative colitis

A

15-25 years and in those aged 55-65 years.

123
Q

where does ulcerative colitis occur in the GI tract

A

starts at rectum (hence this is the most common site for UC), never spreads beyond ileocaecal valve and is continuous

124
Q

what are the investigations for ulcerative colitis

A
  • colonoscopy and biopsy for diagnosis
    • however there is high risk of perforation in severe disease so flexible sigmoidoscopy is preferred
  • Barium enema
125
Q

what do you find on endoscopy in ulcerative colitis

A
  • red, raw mucosa, bleeds easily
  • no inflammation beyond submucosa
  • widespread superficial ulceration which has the appearance of polyps (‘pseudopolyps’)
  • inflammatory cell infiltrate in lamina propria
  • neutrophils migrate through the walls of glands to form crypt abscesses
  • depletion of goblet cells and mucin from gland epithelium
126
Q

what do you see on barium enema of ulcerative colitis

A
  • loss of haustrations
  • superficial ulceration, ‘pseudopolyps’
  • long standing disease: colon is narrow and short -‘drainpipe colon’
127
Q

name some extra-intestinal disease features that are common to both ulcerative colitis and crohn’s

A
  • arthritis (most common in both CD and UC)
  • erythema nodosum
  • episcleritis (more common in CD)
  • osteoporosis
  • uveitis (much more common in UC)
  • pyoderma gangrenosum
  • clubbing
  • PSC (much more common in UC)
128
Q

how do you grade the severity of a flare of ulcerative colitis

A
  • Mild
    • fewer than 4 stools per day
    • no systemic disturbance
    • normal CRP and ESR
  • Moderate
    • 4-6 stools per day
    • minimal systemic disturbance
  • Severe
    • more than 6 stools per day
    • some evidence of systemic disturbance
      • tachycardia
      • abdominal tenderness
      • anaemia
      • fever
      • hypoalbuminaemia
129
Q

how do you induce remission in ulcerative colitis

130
Q

how do you maintain remission in ulcerative colitis

131
Q

what is the aetiology of hepatic encephalopathy

A

not fully understood but involves excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut

132
Q

how do you grade hepatic encephalopathy

A
  • Grade I: Irritability
  • Grade II: Confusion, inappropriate behaviour
  • Grade III: Incoherent, restless
  • Grade IV: Coma
133
Q

how is hepatic encephalopathy treated

A

lactulose with rifaximin for the secondary prophylaxis of hepatic encephalopathy

  • lactulose promotes excretion of ammonia
  • antibiotics such as rifaximin modulate the gut flora resulting in decreased ammonia production
134
Q

what is the definition of malnutrition

A
  • a BMI of less than 18.5; or
  • unintentional weight loss greater than 10% within the last 3-6 months; or
  • a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
135
Q

what is the most common type of oesophageal cancer

A
  • Until recently it was squamous cell carcinoma
  • Adenocarcinoma is now the most common type of oesophageal cancer
  • Adenocarcinoma is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s.
136
Q

what is the difference between squamous cell carcinomas and adenocarcinomas of the oesophagus with reference to their epidemiology, location and risk factors

137
Q

presenting features of oesophageal cancer

A
  • dysphagia: the most common presenting symptom
  • anorexia and weight loss
  • vomiting
  • other possible features include: odynophagia, hoarseness, melaena, cough
138
Q

how do you diagnose oesophageal cancer

A
  • endoscopy and biopsy
  • CT chest abdo pelvis for initial staging
139
Q

management of oesophageal cancer

A
  • Operable disease is managed by surgery
    • Most common is an Ivor-Lewis type oesophagectomy
    • The biggest challenge is anastomotic leak - an intrathoracic anastomosis resulting in mediastinitis
  • In addition to surgical resection many patients will be treated with adjuvant chemotherapy
140
Q

gastric cancer symptoms

A
  • epigastric pain
  • dysphagia (especially if cancer in proximal stomach)
  • dyspepsia
  • weight loss
  • anorexia
  • overt upper GI bleeding in a minority
  • if lymphatic spread
    • virchow’s node (left supraclavicular lymph node)
    • periumbilical nodule
141
Q

what investigations for gastric cancer

A
  • diagnosis: endoscopy with biopsy
    • Signet ring cells may be seen in gastric cancer.
    • Higher numbers of signet ring cells are associated with a worse prognosis
  • staging: CT
142
Q

what is Courvoisier’s law

A
  • Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
143
Q

presenting features of pancreatic cancer

A
  • classically painless jaundice
    • pale stools, dark urine, and pruritus
    • cholestatic liver function tests
  • however, patients typically present in a non-specific way:
    • anorexia
    • weight loss
    • epigastric pain
  • loss of exocrine function (e.g. steatorrhoea)
  • loss of endocrine function (e.g. diabetes)
  • atypical back pain is often seen
144
Q

oesophageal causes of gi bleeding

A

mallory weiss tear

oesophageal varices

oesophageal cancer

oesophagitis

145
Q

gastric causes of gi bleeding

A

dieulafoy lesion

gastric cancer

gastric ulcer

diffuse erosive gastritis

146
Q

duodenal causes of gi bleeding

A

Duodenal ulcer - erosion of gastroduodenal artery

Aorto-enteric fistula - can be de-novo but usually secondary to an abdominal aortic aneurysm repair

147
Q

two risk assessment scores for upper GI bleeding

A

Glasgow-Blatchford bleeding score (GBS) is a screening tool to assess the likelihood that a person with an acute upper gastrointestinal bleeding (UGIB) will need to have medical intervention such as a blood transfusion or endoscopic intervention

Rockall risk scoring system attempts to identify patients at risk of adverse outcome following acute upper gastrointestinal bleeding - it’s for after they’ve had their endoscopy

148
Q

what does intrinsic factor help to absorb

149
Q

which cells secrete intrinsic factor

A

parietal cells in the stomach

150
Q

causes of b12 deficiency

A
  • pernicious anaemia: most common cause
  • post gastrectomy
  • vegan diet or a poor diet
  • disorders/surgery of terminal ileum (site of absorption)
    • Crohn’s: either diease activity or following ileocaecal resection
  • metformin (rare)
151
Q

features of vitamin b12 deficiency

A
  • macrocytic anaemia
  • sore tongue and mouth
  • neurological symptoms
    • the dorsal column is usually affected first (joint position, vibration) prior to distal paraesthesia
  • neuropsychiatric symptoms: e.g. mood disturbances
152
Q

what is the management for b12 deficiency in those who have no neurological involvement

A
  • Initially administer hydroxocobalamin 1 mg intramuscularly three times a week for 2 weeks.
  • The maintenance dose depends on whether the deficiency is diet related or not. For people with B12 deficiency that is:
    • Not thought to be diet related — administer hydroxocobalamin 1 mg intramuscularly every 2–3 months for life.
      • vegans may need this too
    • Thought to be diet related — advise people either to take oral cyanocobalamin tablets 50–150 micrograms daily between meals, or have a twice-yearly hydroxocobalamin 1 mg injection.
      • advice on diet - eggs and meat

IF THEY’RE ALSO FOLATE DEFICIENT THEN TREAT THE B12 DEFICIENCY FIRST OTHERWISE YOU COULD CAUSE SUBACUTE COMBINED DEGENERATION OF THE CORD

153
Q

what is the management of B12 deficiency in people with neurological features

A

initially administer hydroxocobalamin 1 mg intramuscularly on alternate days until there is no further improvement,

then administer hydroxocobalamin 1 mg intramuscularly every 2 months.

154
Q

what is the triad for wernicke’s encephalopathy

A

ophthalmoplegia/nystagmus, ataxia and confusion

155
Q

what causes wernicke’s encephalopathy

A

thiamine deficiency which is most commonly seen in alcoholics

156
Q

what is korsakoff’s syndrome

A
  • when wernicke’s (thiamine deficiency) is untreated you can get korsakoff’s as well
  • it’s the addition of anteretrograde amnesia and confabulation
  • therefore the features of wernicke-korsakoff’s are:
    • opthalmaplegia
    • nystagmus
    • ataxia
    • confusion
    • anteretrograde amnesia
    • confabulation
157
Q

what is the cancer marker for pancreatic cancer

158
Q

what is the cancer marker for hepatocellular carcinoma

A

alpha fetoprotein

159
Q

management of c difficile

A

First episode: oral vancomycin
Second or subsequent episode of infection: oral fidaxomicin

160
Q

management of campylobacter enteritis

A

Clarithromycin

161
Q

managment of shigellosis

A

Ciprofloxacin

162
Q

managment of salmonella

A

Ciprofloxacin

Finals (19 decks)

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